Effects of Anes on CV Flashcards
1
Q
What are the 3 most commonly used IAs?
A
Sevo, Iso, Des
2
Q
What is the primary effect of anesthesia on the CV system?
A
Anesthetics are myocardial depressants
3
Q
In general, circulatory effects are _____ dependent and ______specific
A
Dose; Drug
4
Q
Is N2O a minimal, mild or moderal cardiac depressant?
A
Mild
5
Q
Referring to N2O:
- is myocardial contractility increased or decreased?
- is intracellular Ca more or less available during contraction?
A
decreased; less available
6
Q
What is the effect of N2O on HR? What receptor can be stimulated?
A
Tachycardia - causes a sympathomimetic response; Alpha.
7
Q
Does NO change SVR?
A
NO, no it does not.
8
Q
What is the effect of N2O on CO?
A
Can decrease or increase due to changes in HR
9
Q
Does N2O increase PVR & RAP? Does it cause pulmonary HTN?
A
Increase; yes, from increased PVR
10
Q
Does N2O cause dysrthmias? Does it compromise coronary blood flow?
A
No
11
Q
Do IAs cause myocardial depression? Do IAs increase or decrease Ca entry into the cell?
A
Depression; decrease
12
Q
How do IAs alter the release and uptake of the Ca in the SR?
A
reduce
13
Q
How do IAs alter the kineteics of Ca release and uptake?
A
Decrease sensitivity of contractile proteins to calcium
14
Q
Do IAs potentiate coronary steal? Which IA is the largest contributor?
A
Yes; ISO!
15
Q
Do IAs increase coronary bloodflow?
A
Yes, all but Halothane
16
Q
What is coronary steal?
A
Upon vasodilation, blood is diverted to areas of good perfusion from those of poor perfusion due to inability to dilate.
17
Q
Which IA increases collateral blood flow when aortic pressure is held constant?
A
Sevo
18
Q
Enflurane, Halothane, Isoflurane, Des, and Sevo cause _____ dependent myocardial depression
A
dose
19
Q
Enflurane, Halothane, Isoflurane, Des, Sevo: Is myocardial contractility increased or decreased
A
decreased
20
Q
Which agent has the GREATEST effect of depressing Ca influx and SR release during depolarization?
A
ENFLURANE!
21
Q
Does enflurane have a possible vagolytic effect?
A
yes
22
Q
Does enflurane attenuate atropine?
A
Yes
23
Q
Does enflurane change HR? If so, what is the effect?
A
No but may slightly increase
24
Q
What is the effect of Enflurance on SVR and CO?
A
Reduces both
25
How does enflurane affect RAP? And PVR?
Increase RAP; No change to SVR
26
How does eflurane increase CBF?
Increases activation ATP sensitive K channels and stimulates adenosine receptors
27
Which agent decrease BP more, enflurane or halothane?
enflurane
28
Order these from highest to lowest in regards to cause of arrhythmia: iso, enflurane, halothane?
Halothane>Enflurane > isoflurane
29
Do enflurane, isoflurane, des, and sevo attenuate the baroreceptor response and vasomotor reflex response?
Yes
30
At 2 MAC, how much will halothane reduce BP and CO?
50%
31
How is HR reduced with halothane?
depresses the SA node pacemaker and depresses SNS outflow and causes increased conduction delay through AV nodal pathway
32
Are SV, CO, and BP reduced in halothane use?
Yes
33
How is BP reduced with halothane use?
Reduces contractility and CO. Inhibition of baroreceptor response
34
What medication can be used to combat reduced BP in Halothane use?
Ca chloride
35
Is Halothane extremely arrhythmogenic?
YES!
36
If SVR is decreased in Halothane use, waht is the cause?
2/2 reduced sympathetic tone and CO
37
Does PVR increase, decrease, or not change in Halothane use?
not change
38
Does RAP increase with Halothane use?
yes
39
Why do we see an increase in arrythmiaas in the use of halothane?
The myocardium becomes sensitized to catecholamines. Interferes with Ca channel conduction resulting in prolonged QT
40
If HR does increase with Iso use, what is the cause? What population is this most common in?
Due to the the reduction in vagal tone or compensatory response to reduced SVR; Young healthy patients
41
Is there partial or full preservation of the baroreceptor reflex with Iso use?
partial baroreceptor reflex preservation
42
With Iso, is SV decreased, increased or no change? What about CO and BP?
decreased. May see no change in CO
43
Is the level of CO depression with Iso use similar or different to that of sevo and Des?
similar
44
Which cause greater BP decrease: iso or halothane?
Iso
45
Which has a greater decrease in SVR: Iso or Enflurane?
Iso
46
Do Iso and Des cause a change in PVR? What about RAP?
No; Yes, increases it
47
Do Iso and Des cause arrhythmias?
No
48
Des at <1 MAC results in ____ in HR
No change
49
Des at >1 MAC results in ____ in HR
increase/tachycardia
50
Des: are SV, CO, and BP decreased?
decreased
51
A rapid increase in concentration of Des results in a transient _____ in HR, BP, and catecholamine levels
increase
52
Does Des cause reduced SVR?
Yes, potent vasodilator at increased doses
53
Do Des and Sevo cause change to coronary blood flow/cause coronary steal?
No
54
Are the circulatory effect of Des similar to that of Iso?
Yes
55
Sevo < 1.5 MAC causes _____ to HR
no change
56
Sevo > 1.5 MAC causes _____ to HR
increase, especially in the pediatric population
57
Does Sevo decrease SV, CO or BP?
decreases all
58
Order these based on SVR decrease: Iso, Sevo, Des
Iso=Des>Sevo
59
Does Sevo cause change to PVR & SVR?
No change
60
Does Sevo cause dysrrhythmias?
No
61
Are the circulatory effects of sevo similar to iso and halothane?
yes
62
Order these in regards to increase to HR: S, D, I, H
D>I>S>H
63
Order these in regards to greatest drop in MAP: S, D, I, H
H>ISD
64
Order these in regards to greatest drop in MAP: S, D, I, H
H>D>S=I
65
Order these in regards to greatest drop in SVR: S, D, I, H
D>I>S>H where halothane maintains a decently steady SVR
66
Does Sevo increase, decrease or have no to RAP?
no change. All other IAs, inluding NO, increase
67
Which IAs are most arrythmogenic? Which are least arrythmogenic
H>E where I,S,D have little to no arrhythmic tendency
68
Order these in regards to decreased in myocardial contractility: I,D,E,H,S
E>>>H>I, S, D (dose dependent)
69
Which IAs have an increase in HR at >1 MAC
I, D, E
70
Which IAs maintain HR at 1 MAC?
S, H
71
Which IA causes the greatest SV decrease?
Enflurane!
72
Which IAs cause decrease in CO?
H, E
73
Which IAs cause slight to no decrease in CO?
I, S, D
74
Order these IAs from greatest decrease in SVR to least: S,I,H,D,E
I, E, D>S,H
75
Order these IAs in regards to coronary blood flow change/coronary steal: H,I,E
I>>E,H
76
Which IAs do not cause changes to coronary blood flow/coronary steal
S, D
77
Does sodium thiopental cause direct myocardial depression?
yes
78
How does the induction dose of Sodium thiopental effect SVR, Contractility, and HR?
Decrease SVR & CO; increase HR
79
What center in the brain is depressed by sodium thiopental resulting in venodilation/decreased venous return
medullary vasomotor center
80
Does sodium thiopental reduce sympathetic outflow? Does sodium thiopental have a central vagolytic effect?
Yes; yes
81
Is the baroreceptor reflex mainitanied with sodium thiopental administration? If so, what does it do?
Yes, it helps maintain CO
82
Methohexital is how many times MORE potent that sodium thiopental?
3x
83
Does methohexital have a histamine release? Is it likley to cause arrythmias?
NO; no
84
Does methohexital cause venodilation and myocardial depression?
Yes; yes
85
Does methohexital have RAPID recovery?
YES!
86
Which has more CV stability and by how much: Sodium thiopental vs etomidate
etomidate, 4X
87
Does etomidate change CO or contractility?
NO
88
Why might you see a slight (very min) drop in BP after admin?
due to slight decrease in SVR
89
Does etomidate cause SNS outflow reduction?
Yes
90
Does etomidate have a histamine release?
NO
91
What is the most significant adverse effect of etomidate?
transient inhibition of adrenal steroid synthesis.
92
A single dose of etomidate causes dose dependent inhibition of what enzyme for 6-12 hrs? Why is this a concern?
11 beta hydroxylase; this will result in a reduced stress response
93
What is 11 beta hydroxylase responsible for?
Responsible for converting 11-deoxycortisol to cortisol (adrenocortical suppression
94
About how long did it take for patient's adrenal suppression to resolve post etomidate induction?
approx 48 hrs
95
Which has more hypotension: Sodium thiopental vs propofol
propofol
96
Propofol increases or decreases SVR/contractility/preload?
decreases
97
Which has more HR compensation: Sodium thiopental vs propofol? Why?
Sodium thiopental because propofol impairs arterial baroreceptor response to hypotension
98
In what patient populations (3) should propofol be used cautiously?
CV diseased patients, elderly, and volume depleted patients (dehydration).
99
Propofol induces the release of _____ and acts as a ______ blocker and activates _______ leading to a decrease in ______ & _______
NO; CCB; Protein kinase C; CO & arterial pressure
100
Does Ketamine cause SNS outflow? Does it or does it not mimic SNS stim?
Yes, profound; does mimic
101
What is the effect of ketamine on NE? Does ketamine increase or decrease BP/HR/CO?
Inhibits the reuptake of NE; increases
102
Does ketamine cause indirect stimulation? Does ketamine have direct negative or positive inotropic effects?
Yes; direct negative by inhibitng Ca influx into cardiac myocytes
103
What is the effect of ketamine on MVO2, arrythmias, and PA pressures
increases all
104
In what conditions (3) is ketamine helpful?
shock/traumas, tamponade, restrictive pericaridits
105
What conditions (2) should ketamine be used be w/caution?
Patients with catecholamine depletion (may potentiate the neg inotropic effects) and CAD
106
Dexmedetomidine is a selective _____ adrenergic agoinst. ______ the release of NE. _____ hemodynamic stability
alpha 2; inhibits; increases
107
What are the 2 main side effects of dex?
dose dependent bradycardia and hypotension
108
What is the loading dose of dex? What is the maintenance dose?
0.5-1 mcg/kg; 0.2-0.7 mcg/kg/h
109
Can dex be cardio protective post MI or arrhythmia related injury?
Yes
110
Are benzos cardiac stable? Benzos _____ SAP & _____ HR? Do they have minimal or maximal direct effects on myocard/cystemic circ?
yes; decrease & increase as compensatory; min
111
Hemodynamic changes with benozos are seen in _____ with other drugs?
combination
112
Order these from most potent to least: midaz, loraz. diaz
lorarz>midaz>diaz
113
What is the induction dosing for midaz?
0.1-0.4 mg/kg
114
Diazepam vs Midaz: Which causes a larger BP drop? Which causes compensatory increas to drop in vagal tone, more?
Midaz; midaz
115
Does midaz cause CO changes?
no
116
What is the BZD antag? What is the initial IVP dose up to max? What is the IV infusion dose?
Flumazenil; 0.2 mg/min up to 1 mg; 8-15 mcg/kg
117
Does flumazenil affect BP/HR/LV systolic function? Does it affect hemodynamics in those with CAD
NO
118
N2O + Opioid = ___ depression
CV
119
Opioid + Benzodiazepines = _____ SVR and BP
decreased
120
What are examples of opioid agonists?
Morphine, Fentanyl, Sufentanil, Alfentanil, Remifentanil Meperidine, Methadone
121
Are the fentanyls, meperidine ad methadone relatively CV stable?
yes
122
Do opioid agonists blunt SNS outflow? Do the fentanyls, meperidine ad methadone have a histamine release?
yes; no
123
How do the fentanyls, meperidine ad methadone reduce HR? Which has the most prominent HR reduction effect? Morphine vs fentanyl: which decrease HR more?
cause central vagal excitation and depress cardiac conduction > prolonged purkinje fiber AP duration; sufentanil; fentanyl
124
Amongst fentanyls, meperidine ad methadoneopioid, which actually increase HR and why?
Meperidine because it has a similar structure to atropine
125
What routes can morphine be administered? Why do you see a BP decrease with morphine and dilaudid?
IV or intrathecal; large histamine release/blunted SNS outflow/venodilation
126
Why does morphine and dilaudid reduced HR?
Yes, causes reduced SNS outflow & central vagal excitation
127
Methadone _____arterial blood pressure and ______ arterial partial pressure of carbon dioxide
Increases;increases
128
Methadone ______HR and pH. Methdaone _____NMDA
increased; antagonizes
129
What is the dosiing of methadone? Is the 1/2 life of methadone long or short? What is it?
0.15mg/kg; long; 24-36 hrs
130
What are the (3) main cardiac risks associated with methadone?
increased risk of QT prolongation, torsade de pointes, and cardiac death-directly related to dose and chronic use
131
Does morphine cause myocardial sensitization? Why is it important to maintain preload when using morphine?
No; patients are at risk for orthostatic hypotension with position change
132
Meperidine is ____as potent as morphine and acts a ____myocardial depressant and _____CO/SNS activity (contractility & SVR) and ____HR/histamine release
1/10th; direct; reduces; increases
133
Naloxone is an opioid _____. Naloxone _____ SNS activity/HR/BP/cardiac dysrthmias
antagonist; increases
134
What are 2 medical risks associated with narcan administration?
Narcan induced noncardiogenic pulmonary edema & Adrenergic crisis secondary to catechole surge
135
Nalbuphine is an opioid ______. Does or does not cause adverse cardiac/parameter changes?
agonist/antagonist; does not
136
Succinylcholine can cause what cardiac rhythm issues?
Sinus Bradycardia, Junctional Rhythm, Sinus Arrest - particularly with 2nd dose
137
What is the active metabolite of succinycholine? How does it cause rhythm changes?
Succinylmonocholine which sensitize M2 cholinergic receptors in the SA node
138
What can cause increased HR with succinylcholine administration? Can succs increase/decrease BP?
Action at sympathetic ANS ganglia once stimulated; yes
139
Does Roc have a histamine release or vagolytic effect?
No
140
Does pancuronium cause SNS activation (increase HR/CO/BP/SVR)?
Yes
141
Is pancuronium a selective cardiac vagal blocker? If so, when is it more pronounced?
Yes; with altered AV conduction
142
Does pancuronium cause increase in AV conduction/have a catecholamine release? Is there a histamine release?
yes; no
143
Does Atracurium have a direct effect on myocardium? When would you see a histmaine release?
No; in large dose administration
144
What medications are used for NDMR reversal? What is the predominant negative effect?
cholinergic agents (neostigmine) with anticholinergics (glyco) to offset bradycardia
145
Does sugammadex affect hemodynamic values? Can people have anaphylaxis?
No; yes
146
Non cardiac CAD cases:
what preop meds?
What induction med?
What MR, why?
What maintenance IA?
What emergency meds?
What other med to consider?
preop: midaz, fent
induction: etomidate or prop MR: roc bc risk of bradycardia with succs
IA: iso potentially - careful with coronary steal
Emergency meds: ephedrine, phenylephrine, epinephrine, lidocaine, atropine, nitroglycerine
What other med to consider: metoprolol
147
What is entailed in a cardiac stress related response in a CAD patient?
catecholamine release, tachycardia, hypertension, ischemia and increased MvO2 >Upper airway obstruction, hypoxemia/hypercarbia and acidosis
148
Avoid or Use In CAD patients: ketamine vs dex, long or short laryngoscopy? Post-induction hypotension?
avoid ketamine/use dex, short/atraumatic intubation, avoid post induction hypotension
149
What are some advantages to using narcs with CAD patients?
cardiac stablity is maintained, reduce HR, avoids coronary steal
150
Why use narcs in patients with good LV CAD?
If not used; pt with good LV function may respond with hypertension and tachycardia to surgical stimulation
151
What are some disadvantages to using narcs with CAD patients?
predictable hypotension, poor titratability, and potential for recall
152
What are some advantages to using IAs with CAD patients?
dose dependent negative inotropic effects, titratable, induces amnesia, reliable, I=S=D
153
What are some disadvantages to using IAs with CAD patients?
Dose-related negative inotropic effects, Myocardial depression, Systemic hypotension, Lack of postop analgesia
154
Is it better to pain IAs with narcotics for patients with CAD?
YES, may produce advantages and minimal undesirable effects
155
Why is pain management so important postop for CAD patients?
Pain > increases SNS stimulation > increased HR/ MvO2
156
What are the hemodynamic goals for CAD patients?
maintain preload/afterload, contractility depression if ok LV, slow HR, NO arrhythmias, keep MVO2 low
